中文摘要：

工具包 W-2Bao 老鼠是有在我们的实验室被引起的一个 B6 背景的单个基因的正染色体的主导的变化老鼠。而同质接合体有身体，黑眼睛，和不孕的白化病，异质接合体包括腹部，极限，和尾巴的白化病有词法特征。同型结合的异种出现了小，在结构上反常性腺，和缺乏的细菌房间。异质接合的雄的老鼠在一些曲解的生精的小管缺乏细菌房间。这个变化在由连接分析的染色体 5 从着丝点在 43.8 厘米被印射，工具包作为候选人基因被识别了。在工具包全身的 mRNA 扩大以后，到在在 ORF 的位置 1228 点的 T 变换的 G 从 V 把第 410 氨基酸改变了到 F，这被发现。这个氨基酸变化能影响蛋白质第二等的结构。异质接合的变异的老鼠被交叉，同型结合的变异的老鼠被饲养并且 genotyped。我们发现初发的细菌房间(PGC ) 都没在在同质接合体的胎儿白天 11.5 点出现在尿生殖的山脉区域。PGC 的数字显著地也在异质接合体减少了。在胎儿白天 15.5 点，睾丸小管结构的区别是不清楚的；也，他们没包含 spermatogonia。女同质接合体没在卵巢包含初发的滤泡。PGC 和初发的滤泡的数字显著地在异质接合的老鼠被减少。W ? 2Bao 是唯一的变异的地点在细胞外第 4 象 Ig 一样领域和这个变异的鼠标模型为繁殖系统开发的机制的学习提供新材料。

英文摘要：

Kit^W-2Bao mice are single-gene autosomal dominant mutation mice with a B6 background that were bred in our laboratory. Heterozygotes had morphological characteristics including albinism of the abdomen, extremities, and tail, whereas the homozygotes had albinism of the body, black eyes, and infertility. The homozygous mutants showed small, structurally abnormal gonads, and lacked germ cells. Heterozygous male mice lacked germ cells in some contorted seminiferous tubules. This mutation has been mapped at 43.8 cM from the centromere in chromosome 5 by linkage analysis and Kit has been identified as the candidate gene. After Kit full-length mRNA amplification, it was found that a G to T conversion at position 1228 in the ORF changed the 410th amino acid from V to F. This amino acid change could affect the protein＇s secondary structure. Heterozygous mutant mice were intercrossed and homozygous mutant mice were bred and genotyped. We found that no primordial germ cells （PGCs） appeared in the urogenital ridge area at fetus day 11.5 in the homozygotes. The number of PGCs also significantly decreased in heterozygotes. At fetus day 15.5, the differentiation of the testis tubule structure was unclear; as well, they contained no spermatogonia. Female homozygotes contained no primordial follicles in the ovary. The numbers of PGCs and primordial follicles were significantly decreased in heterozygous mice. W^2Bao is the only mutated site in the extracellular 4th Ig-like domain and this mutant mouse model provides new material for the study of the mechanism of reproductive system development.